SHOCK Dr.Mohammed Sharique Ahmed Quadri Assistant Prof.Physiology Almaarefa College

WHAT IS SHOCK? Shock is the term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia and/or an inability of the cells to utilize oxygen. SHOCK IS A SYNDROME THAT CAN OCCUR IN THE COURSE OF MANY LIFE THREATENING TRAUMATIC CONDITIONS OR DISEASE STATES 2

Or it can be define simply as A clinical state in which tissues do not receive adequate blood flow and O2 to meet their metabolic needs. 3

Physiological Principles MAP = CO X PVR CO – Cardiac Output PVR – Peripheral Vascular resistance Tissue perfusion is driven by mean arterial pressure MAP 4

Cardiac Output CO = SV X HR This means that MAP= SV X HR X PVR Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance MAP= DP+ 1/3 PP and normal value for adult is between 60 and 110 mm Hg Normal adult CO is about 5 L/ min& is equal for both ventricles 5

Stroke Volume Volume of Blood pumped by the heart during 1 cycle What affects Stroke volume? Heart Muscle Damage Blood Volume Mechanical Obstruction Rhythm Problems 6

What makes up blood volume 7 Plasma RBCs WBCs Platelets

What Alters Blood Volume? Haemorrhage Plasma Loss Loss /Redistribution of Extracellular Volume 8

Heart Rate Heart rate increases as a compensatory response to Shock Heart rate too fast to allow adequate refilling of heart between beats 9

Peripheral Vascular Resistance PVR regulated by ARTERIOLAR tone. Dilatation opens Arteriovenous beds & increases volume of circulatory system 10

What Alters PVR? Circulating cytokines & Inflammatory mediators (e.g. Histamine) Endotoxins Drugs (e.g. Nitrates) 11

So tissue and cellular perfusion is dependent on Adequate preload Functioning heart Intact blood vessels 12

TYPES OF SHOCK HYPOVOLEMIC CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE 13

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Pathophysiology: Overview Tissue perfusion is determined by Mean Arterial Pressure (MAP) MAP = CO x SVR Heart rateStroke Volume

Hypovolemic Shock: Pathophysiology Heart pumps well, but not enough blood volume to pump MAP = CO x SVR HR x Stroke volume

Hypovolemic Shock: Pathophysiology Normal MAP = CO x SVR Hypovolemic MAP = ↓ CO x SVR MAP = ↓ CO x ↑ SVR ↓ MAP = ↓↓ CO x ↑ SVR

Hypovolemic Shock: Causes ↓ MAP = ↓ CO (HR x Stroke Volume) x ↑ SVR Decreased Intravascular volume (Preload) leads to Decreased Stroke Volume – Hemorrhagic - trauma, GI bleed, AAA rupture, ectopic pregnancy – Hypovolemic - burns, GI losses, dehydration, third spacing (e.g. pancreatitis, bowel obstruction), Adesonian crisis, Diabetic Ketoacidosis

Cardiogenic Shock: Pathophysiology Heart fails to pump blood out MAP = CO x SVR HR Stroke Volume

Cardiogenic Shock: Pathophysiology Heart fails to pump blood out MAP = CO x SVR HR Stroke Volume

Cardiogenic Shock: Pathophysiology Normal MAP = CO x SVR Cardiogenic MAP = ↓ CO x SVR MAP = ↓ CO x ↑ SVR ↓ MAP = ↓↓ CO x ↑ SVR

Cardiogenic Shock: Causes ↓ MAP = ↓ CO (HR x Stroke Volume) x ↑ SVR Decreased Contractility (Myocardial Infarction, myocarditis, cardiomypothy, Post resuscitation syndrome following cardiac arrest) Mechanical Dysfunction – (Papillary muscle rupture post-MI, Severe Aortic Stenosis, rupture of ventricular aneurysms etc) Arrhythmia – (Heart block, ventricular tachycardia, SVT, atrial fibrillation etc.) Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)

Obstructive Shock: Pathophysiology Heart pumps well, but the output is decreased due to an obstruction (in or out of the heart) MAP = CO x SVR HR x Stroke volume

Obstructive Shock: Pathophysiology Normal MAP = CO x SVR Obstructive MAP = ↓ CO x SVR MAP = ↓ CO x ↑ SVR ↓ MAP = ↓↓ CO x ↑ SVR

Obstructive Shock: Causes ↓ MAP = ↓ CO (HR x Stroke Volume) x ↑ SVR Heart is working but there is a block to the outflow – Massive pulmonary embolism – Aortic dissection – Cardiac tamponade – Tension pneumothorax Obstruction of venous return to heart – Vena cava syndrome - eg. neoplasms, granulomatous disease – Sickle cell splenic sequestration

Distributive Shock: Pathophysiology Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone MAP = CO x SVR HR x Stroke volume

Distributive Shock: Pathophysiology Normal MAP = CO x SVR Distributive MAP = co x ↓ SVR MAP = ↑ co x ↓ SVR ↓ MAP = ↑ co x ↓↓ SVR

Distributive Shock: Causes ↓ MAP = ↑ CO (HR x SV) x ↓ SVR Loss of Vessel tone – Inflammatory cascade Sepsis and Toxic Shock Syndrome Anaphylaxis Post resuscitation syndrome following cardiac arrest – Decreased sympathetic nervous system function Neurogenic - C spine or upper thoracic cord injuries – Toxins Due to cellular poisons -Carbon monoxide, methemoglobinemia, cyanide Drug overdose (a1 antagonists)

PATHOPHYSIOLOGY OF SHOCK The manifestation of shock reflects both – The impaired perfusion of body tissue & – The body’s attempt to maintain tissue perfusion (compensatory mechanism) 29 So the pathophysiology of shock can be explained as cellular hypoxia resulting from impaired tissue perfusion

COMPENSATORY MECHANISMS 30

Compensatory mechanism and shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD 31

Hypovolaemic shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD 1 32

Hypovolaemic shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD 1 33

Hypovolaemic shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD

Cardiogenic shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD 1 35

Cardiogenic shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD

Cardiogenic shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD

Distributive shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD 1 38

Distributive shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD 21 39

Distributive shock Fluid Volume (CVP/JVP) Vascular Diameter (SVR) Cardiac Output (SV x HR) PRE-LOAD AFTER-LOAD

Type of Shock InsultPhysio logic Effect Compen sation Heart Rate Compensation Contractility CardiogenicHeart fails to pump blood out ↓ COBaroRc ↑ SVR ↑↑ ObstructiveHeart pumps well, but the outflow is obstructed ↓ COBaroRc ↑ SVR ↑↑ HemorrhagicHeart pumps well, but not enough blood volume to pump ↓ CO BaroRc ↑ SVR ↑↑ DistributiveHeart pumps well, but there is peripheral vasodilation ↓ SVR ↑ CO ↑ No Change - in neurogenic shock ↑ No Change - in neurogenic shock

Sympatho-Adrenal Response to Shock Most immediate of compensatory mechanisms are those of sympathetic nervous system and renin angiotensin mechanism Sympathetic nervous system NE, epinephrine, and cortisol release Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) Renin-angiotensin axis Water and sodium conservation and vasoconstriction Increase in blood volume and blood pressure 42

Sympatho-Adrenal Response to Shock 43

Neuroendocrine response Release of pituitary hormones such as adrenocorticotrophic hormone (ACTH), vasopressin(antidiuretic hormone, ADH). There is release of cortisol, which causes fluid retention and antagonizes insulin. There is release of glucagon, which raises the blood sugar level. 44

Release of Pro- and Anti Inflammatory Mediators Severe infection (bacteraemia/endotoxaemia), Presence of large areas of damaged tissue (following trauma /extensive surgery) Prolonged episodes of hypoperfusion 45 Trigger an exaggerated inflammatory response (systemic activation of leucocytes & release of potentially damaging ‘mediators’)

Release of Pro- and Anti Inflammatory Mediators (continued) Pro inflammatory Mediators: – Proteases – Toxic free radicals & other reactive oxygen species – Cytokines IL TNF – Platelet activating factor Hypotension, Inc. vascular permeability, platelet aggregation. Anti inflammatory mediators: – Interleukin 10 ( IL-10) 46 Are involved in leukocyte adhesion,local inflammation, neutrophil activation, fever, lactic acidosis, ventilation perfusion abnormalities

Release of Pro- and Anti Inflammatory Mediators (continued) Although beneficial when targeted against local areas of infection or necrotic tissue-- dissemination of this ‘innate immune’ response can produce shock and widespread tissue damage. Characteristically the initial episode of overwhelming inflammation is followed by a period of immune suppression--- increased risk of developing secondary infections. 47

TO BE CONTINUED TOMORROW THANK YOU 48

CLINICAL FEATURES OF SHOCK 49

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THANK YOU 54 Reference Kumar & Clark's Clinical Medicine, 7th Edition